VO2 max is a measurement of the maximum amount of oxygen someone can take in and use. It is generally understood that everyone has a ceiling hard-wired into them and that you can approach your body's ceiling with several months of decent endurance training. After that you can't do much more than dick around the edges. http://www.setma.com/article.cfm?ID=137

The anaerobic threshold - or lactate threshold - is not your vo2 max. It's can be expressed as a percentage of vo2 max but it will vary greatly depending on individual training. I've seen ranges of 30 - 70%.

As a practical matter, unless you are an endurance athlete you don't really need to know too much about VO2 max because its not particularly sports specific and you tend to get as much as you need from regular training. (For the same reason a marathon runner doesn't need to know how to train for 1RM in the weight room).

Lactate threshold training is more useful to understand if you are designing a training program or involved in serious training. But HIIT training, Randy Couture's circuit training, fartlek, and rolling at the end of class in five minute segments all tend to improve lactate threshold.

And, for the record, you were completely right to call me out on the 45 seconds.

45 seconds is the approximate amount of time it takes a good Division 1 male college swimmer to "hit the wall' - come to the point where it looks like they are dragging a piano - when they swim without breathing at 100 meter race pace. You can find the reference *I think* in Doc Cousilman's Science of Swimming or Hannula's book on coaching swimming.

I thought it was a pretty good comparison for the original HIIT discussion because its a high intensity event, its controlled for breathing, and I was agreeing with Douglas that HIIIT training is generally more intense and shorter than several minutes on and several minutes off. I still think its a pretty good example.

I do agree that higher intensity effort will burn through your energy supply faster than 45 seconds.

VO2 max is a measurement of the maximum amount of oxygen someone can take in and use.

With you so far.

Originally Posted by dumblucky

It is generally understood that everyone has a ceiling hard-wired into them and that you can approach your body's ceiling with several months of decent endurance training. After that you can't do much more than dick around the edges.

Not sure about this. Finite limits and diminishing returns are reasonable enough in theory, but any time someone says "you can't do much more" I'm immediately skeptical. You probably heard about this study in the news a few months back - it was about the inadequacy of WADA-accredited testing for erythropoietin doping. In the course of their study, they also kept track of a number of other factors, including VO2max. As you might suspect, it increased significantly with EPO injections - and as far as I recall, this is in already well-trained individuals.

All right. Yeah, when I was saying "aerobic threshold", I wasn't referring to what they've called "anaerobic threshold". The term they're using for what I was referring to is "aerobic ceiling".

Originally Posted by dumblucky

The anaerobic threshold - or lactate threshold - is not your vo2 max. It's can be expressed as a percentage of vo2 max but it will vary greatly depending on individual training. I've seen ranges of 30 - 70%.

"The reasons for lactate accumulation are complex and varied and not yet fully understood."

That's disappointing. Something (presumably something not related to lack of oxygen) is impairing oxidative phosphorylation. Even black-box testing should give us some idea as to what that limitation is.

Originally Posted by dumblucky

As a practical matter, unless you are an endurance athlete you don't really need to know too much about VO2 max because its not particularly sports specific and you tend to get as much as you need from regular training. (For the same reason a marathon runner doesn't need to know how to train for 1RM in the weight room).

That's putting it in terms of "training to improve VO2max", but I'm looking at "training with a %VO2max target". The confusion is probably my fault (bad terminology). Backtracking a bit to this post, and swapping "aerobic threshold" with "aerobic ceiling", I think it mostly still holds with what we've established now.

I would speculate that exercise at intensities between the lactate threshold and the aerobic ceiling would have the greatest effect on the aforementioned lactate threshold (whatever the impairment to oxidative phosphorylation is). Assuming that speculation is accurate, "training the aerobic energy systems" and "training to remove an impairment on the aerobic energy systems" should be the same thing.

Originally Posted by dumblucky

Lactate threshold training is more useful to understand if you are designing a training program or involved in serious training. But HIIT training, Randy Couture's circuit training, fartlek, and rolling at the end of class in five minute segments all tend to improve lactate threshold.

Sounds reasonable enough. So I'm curious at this point - what's your best guess as to what the impairment that manifests as the lactate threshold is?

And, for the record, you were completely right to call me out on the 45 seconds.

45 seconds is the approximate amount of time it takes a good Division 1 male college swimmer to "hit the wall' - come to the point where it looks like they are dragging a piano - when they swim without breathing at 100 meter race pace. You can find the reference *I think* in Doc Cousilman's Science of Swimming or Hannula's book on coaching swimming.

I thought it was a pretty good comparison for the original HIIT discussion because its a high intensity event, its controlled for breathing, and I was agreeing with Douglas that HIIIT training is generally more intense and shorter than several minutes on and several minutes off. I still think its a pretty good example.

I do agree that higher intensity effort will burn through your energy supply faster than 45 seconds.

I'll think on this one for a while. It'd be tough to do with swimming, but if they had some sort of ergometer that could show the intensity level before, during and after "hitting the wall", it'd be interesting to look at.

1. EPO is extremely dangerous. It will increase the amount of oxygen you can deliver to your cells, but its not worth it. When you increase hemoglobin in your blood, which is what EPO does, you increase blood density. The danger is that if you take too much EPO you turn your blood into a sludge your heart can't pump. Not too long ago there was a rash of world class cyclists dying in their sleep due to heart failure.

2. There's a practical limit to how much you you normal can increase your VO2 max with normal training in the same way there's a practical limit to how much you can increase your bench 1rm. When you can improve performance by focusing on lactate threshold training, reaching your vo2 max ceiling becomes less important. (Diminishing returns)

3. I think you're on the right track once you change terms.

4. I don't have a real good guess at why impairment happens at the lactate threshold. I tend to think it has to do with acidosis but I'm just following trends.

I was given to understand that what you just said is an old fitness myth and that really, you can only train the rectus abdominus as a whole, not in seperate packets. I suspect that the muscles you primarily train doing a hanging leg raise are your hip flexors rather than your rectus abdominus, which is best trained by doing crunches as that isolates the muscle better.

Can anyone, prefarably somebody with a sports trainer education, clarify this matter?

Well considering I just read it in musclemag a month or so ago, it would be news to them too. I'm not claiming musclemag is the best source for everything but I figured that with the focus on body building and looking good they would know this kind of thing. A good test would be to try the different movements and see where you feel the burn.

EPO is extremely dangerous. It will increase the amount of oxygen you can deliver to your cells, but its not worth it. When you increase hemoglobin in your blood, which is what EPO does, you increase blood density. The danger is that if you take too much EPO you turn your blood into a sludge your heart can't pump. Not too long ago there was a rash of world class cyclists dying in their sleep due to heart failure.

To pick on you for what is fundamentally a reasonable statement, I'm going to underline two things here: "not worth it" and "too much EPO".

Second thing first... too much of anything is a bad thing, and intravenous delivery of chemicals is especially prone to overloading by bypassing the digestive tract's usual rejection mechanisms. The undesirable effects of chemical interventions can be divided into two main categories - direct and incidental. Example:

Testicular atrophy, gyno, and the like are incidental side-effects of anabolic steroids - these problems are not related to the intent of the intervention. An anabolic steroid that did not have these effects would still be useful for athletes for its muscle and strength effects.
The increased rate of injury from the added stress on tendons and bones is a direct side-effect of anabolic steroids, because it is intrinsically connected to the intent (greater muscle size and strength) of the treatment rather than just the means.

We can try (with some success) to work around incidental effects by altering the chemicals used in the interventions, but when it comes to direct effects, we're left to strike a balance between the benefits of the intervention and the complications of said benefits. To stay with the aforementioned example, someone who is using anabolic steroids should 1) moderate their dose strengths and durations to avoid outstripping their tendon growth, 2) adjust their workout plan to avoid high-risk exercises (particularly near-maximal effort) and encourage tendon growth, and 3) adjust their exercise to what their body indicates it can handle. There are similar (but not identical) steps that an athlete supplementing with EPO can take to manage the risk of increased blood viscosity (a direct side-effect). Viscosity is a particularly easy one to track - take a sample of blood and test how thick it is. With pre-supplementation baselines and informed limits of what one's system can handle, the risk can be managed.

Now, as for the first part I highlighted... if a league has banned a particular chemical intervention, then it would be morally wrong for the athlete to make use of said intervention. However, if said chemical intervention is not banned by any organization the individual belongs to, balancing the risks and rewards is a function of the individual's own ethical calculus.

If you had a pill that would guarantee a pitcher twenty wins, but might take five years off his life, he'd take it.

-Jim Bouton, Ball Four

All chemical interventions have risks (from direct side-effects) associated with them. Stimulants and tachycardia, anabolic steroids and cardiac hypertrophy, human growth hormone and cancer. We could push this further - protein and kidney problems, carbohydrates and diabetes. And the next step is to go beyond nutrition and chemistry altogether and look at training in general. Elite-level linemen and sumo wrestlers intentionally put on unhealthy amounts of body fat. The linemen (and football players in general) sustain chronic head trauma as a condition of participation. Elite-level synchronized swimmers have an absolutely obscene rate of knee injury from the "eggbeater" movement. And more relevant to these forums, elite-level judoka land in arguably unsafe ways rather than yielding ippon in competition.

There is a certain point - and this point exists in every sufficiently-developed sport that I know of - where further success in said sport comes at a cost in terms of health risks. When an athlete finds themselves approaching that point, they need to sit down and "do the math" for themselves. How do the risks and rewards balance out? Where does their best shot at a good quality of life lay?

Well considering I just read it in musclemag a month or so ago, it would be news to them too. I'm not claiming musclemag is the best source for everything but I figured that with the focus on body building and looking good they would know this kind of thing. A good test would be to try the different movements and see where you feel the burn.

It is widely believed the lower abs are exercised during the leg raise or other hip flexor exercises. However, it can be misleading to judge the mechanics of an exercise based on localized muscular fatigue. The primary muscle used in hip flexion is actually the Iliopsoas one of many hip flexors. The Iliopsoas, particularly the Psoas portion, happens to lie deep below the lower portion of the Rectus Abdominous. During the leg raise, the entire abdominal musculature isometrically contracts (contracts with no significant movement) to:

o Posture the spine and pelvis
+ Supports the weight of the lower body so the lumbar spine does not hyperextend excessively
+ Maintains optimal biomechanics of the Iliopsoas
# Hips are kept from prematurely flexing if the lumbar spine and pelvis does not hyperextend excessively
# Iliopsoas can contract more forcefully in a relatively slight stretched position
* Bent knee (and hip) sit-ups actually place Iliopsoas at a mechanical disadvantage
o Counteracts Iliopsoas's pull on spine
+ Many people with weak abdominal muscles are not able to perform hip flexor exercises without acute lower back pain or discomfort

The combination of the local muscular fatigue, or a burning sensation from the isometrically contracted abdominal muscles, and from the working hip flexors produces fatigue in the pelvis area which we mistakenly interpret as the lower portion of the Rectus Abdominous being exercised. In movements where the Rectus Abdominous does Isotonically contract (contracts with movement), it flexes the spine by contracting the entire muscle from origin to insertion. The spine is not significantly flexed during the leg raise.

Erythropoietin is neither anabolic nor a steroid, and I haven't represented it as being either. I compared it to anabolic steroids because the latter have been in use for much longer, and we have a clearer picture of their side effects. While we're at it, I also compared it to stimulants, growth hormones, protein and carbohydrates... although technically it does fall into the latter two categories.

Originally Posted by dumblucky

But if you are doing something so earth-shatteringly important that you are willing to inject something that may kill you within 24 hours, knock yourself out.

You'll want to re-read the third-last paragraph of my previous post. If all goes well, I'll be taking my first judo lesson tonight. In judo, as in most contact sports, there is a non-trivial possibility of permanent injury or death.

"But Russ, that's not the same thing."

It is, actually. It's very much the same thing. I had a teammate who played through a neck-shoulder injury in his senior year. Years later, he was rejected for police service because he still hasn't regained full use of his arm. Another friend of mine broke his humerus in a high school game, and he can't lift that arm over his head. Yet another teammate sustained a concussion during practice but hid it and refused to sit out. Later that practice, he took another shot to the head, sustaining lasting impairment to his short-term memory and cognitive ability. He dropped out of school, went to work out on the rigs, and discovered cocaine.

Sports are inherently risky, contact sports especially so. Participating in them is risky. Training for them is risky. We cannot eliminate the risk, only manage it.